- Immune interactions in the regulation of intestinal physiology (e.g. epithelial function). Use of animal models and cell culture to determine if, and then how immune cells (i.e. T cells or monocytes/macrophages) and immune mediators affect epithelial function, particularly active ion transport, barrier properties and cytokine/chemokine production.
- Analysis of direct signal transduction events mobilized in human gut epithelia in response to cytokines, principally interferon-γ(IFNγ) and transforming a growth factor-β (TGFβ) and how the mobilized pathways cross talk to regulate epithelial function.
- Assessment of the impact of pathogenic and non-pathogenic (i.e. commensal or non-noxious) bacteria and bacterial products (e.g. superantigens, CpG-rich DNA) on epithelial physiology, and the role of these agents in modifying gut form and function in rodents.
- Use of animal models of colitis to examine neuronal control of epithelial ion transport.
- Parasitisms as models of gut dysfunction. Examination of how the tapeworm, Hymenolepis diminuta, can prevent or treat a chemically-induced colitis in non-permissive hosts (i.e. helminth is spontaneously expelled) and the permissive rat host where the worm establishes and lives to maturity.